Despite the inherent instability of the CAG repeat within the ATXN7 gene [45], automated fluorescent genotyping of the PCR products indicated that no contractions or large-scale expansions had occurred during either reprogramming or differentiation, consistent with previous reports of other iPSC-derived models of polyQ disorders, including SCA3 and HD [32, 33]. This evidence concerns the gene ATXN3 and Huntington disease.